Changes in the gap junctional intercellular communication in renal tubular epithelial cells in vitro treated with renal carcinogens.
Gap junctional intercellular communications (GJIC) are known as the channels for the direct transfer of cytoplasmic molecules between neighboring cells and are lost during transformation of normal cells. To study the function and the molecular mechanism for the loss of GJIC, the effects of dimethylnitrosamine, KBrO3 and FeSO4 x 7H2O, which are known as chemical tumor promoters of the kidney on the GJIC function and the expression of connexin 43 of Madin-Darby canine kidney (MDCK) epithelial cells, were examined. These tumor promoters inhibited the GJIC in MDCK cells. The expression of connexin 43 mRNA and connexin 43 protein was not altered by these treatments, whereas immunocytochemical study revealed that the distribution of connexin 43 protein was changed from the cell surface to the cytoplasma. These data suggest that blockage of GJIC in MDCK cells treated with renal carcinogens support the hypothesis that loss of GJIC might be important in renal carcinogenesis.
Noguchi
M
M
Department of Urology, Nagasaki University School of Medicine, Japan.
Nomata
K
K
Watanabe
J
J
Kanetake
H
H
Saito
Y
Y
D000818:Animals; D015152:Blotting, Northern; D002273:Carcinogens / Q000633:toxicity*; D002450:Cell Communication / Q000187:drug effects*; D002478:Cells, Cultured; D018031:Connexin 43 / Q000032:analysis / Q000235:genetics; D004285:Dogs; D004847:Epithelial Cells / Q000187:drug effects; D017629:Gap Junctions / Q000187:drug effects*; D007680:Kidney Neoplasms / Q000139:chemically induced*; D007684:Kidney Tubules / Q000187:drug effects*
D002273:Carcinogens; D018031:Connexin 43